1-s2.0-S0733862723000056

C a rd i o v a s c u l a r
C o m p l i c a t i o n s o f P re g n a n c y
a, b a
John Mark Sawyer, MD *, Naseem Moridzadeh, MD , Rebecca A. Bavolek, MD
KEYWORDS
Venous thromboembolism Pulmonary embolism Deep venous thrombosis
Superficial venous thrombosis Acute myocardial infarction
Spontaneous coronary artery dissection Peripartum cardiomyopathy
Aortic dissection
KEY POINTS
The risk of all types of venous thromboembolism increases in the procoagulant state of
pregnancy. This risk increases throughout the duration of pregnancy and into the post-
partum period. Low-molecular weight heparin is the preferred treatment in the setting of
pregnancy.
Pregnancy poses an increased risk for acute myocardial infarction and spontaneous cor-
onary artery dissection. Treatment is similar between the two, with the exception of throm-
bolytics. Ideally, patients should undergo coronary angiography whenever possible.
Peripartum cardiomyopathy is managed similarly to other forms of cardiomyopathy,
including noninvasive ventilation strategies, diuretics, and afterload reduction with
nitroglycerin.
Aortic dissection is a relatively low incidence but high mortality occurrence in pregnancy.
Again, the management is similar to that of the nonpregnant patient, with surgical man-
agement being the preferred modality for Type A dissections and medical management
for Type B dissections.
INTRODUCTION
The physiologic and hormonal changes of pregnancy present significant stress to the
cardiovascular system. Maternal cardiac output increases by 50% and circulating blood
volume may increase by as much as 100% to support the gestating fetus. The hormonal
changes of pregnancy also increase the risk of thrombotic events and vascular dissec-
tions. As maternal age increases in the United States, more women are coming into
pregnancy with significant preexisting conditions that are brought into sharp focus by
these physiologic stresses. The clinical importance of cardiovascular conditions is high-
lighted by the fact that cardiovascular conditions combined with cardiomyopathy
a
UCLA Ronald Reagan, Olive View Emergency Medicine Residency, 1100 Glendon Avenue,
Suite 1200, Los Angeles, CA 90024, USA; b NYU Langone Health, 570 First Avenue, New York,
NY 10016, USA
* Corresponding author.
E-mail address: johnsawyer@mednet.ucla.edu
Emerg Med Clin N Am 41 (2023) 247–258

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248 Sawyer et al
account for 26.5% of pregnancy-related deaths in the United States, making this the
leading cause of such deaths.1 This review—targeted toward the emergency clini-
cian—encompasses the major cardiovascular disorders of pregnancy and highlights
their specific diagnostic challenges and new developments in the field.
VENOUS THROMBOEMBOLISM IN PREGNANCY
For the emergency clinician, the diagnosis and management of venous thromboem-
bolism (VTE) is the most frequently encountered cardiovascular complication of preg-
nancy. VTE includes superficial vein thrombosis (SVT), deep vein thrombosis (DVT),
and pulmonary embolus (PE) with PE being the most challenging diagnosis given
the concern for maternal and fetal exposure to ionizing radiation and differing society
guidelines.2–7 VTE complicates 1.2 per 1000 deliveries and risk increases throughout
pregnancy and into the postpartum period. The postpartum period has a variable defi-
nition but the risk for VTE seems to peak in the first week, declining to the prepreg-
nancy risk after 12 weeks.8
Superficial Vein Thrombosis

Although rarely the primary concern of the emergency clinician approaching a preg-
nant or postpartum patient, SVT may be found in the diagnostic workup of DVT. In
this case, the emergency clinician must assess the risk for a subsequent thrombotic
event or clot extension. Particular attention should be given to SVT above the knee,
extensive SVT (>5 cm), and close proximity to the saphenofemoral junction (within
3 cm) as these are considered higher risk for a subsequent thrombotic event.9–11
The American Society of Hematology recommends treatment with low-molecular
weight heparin (LMWH) for all proven SVT in pregnant patients—this recommendation
was based on studies in the nonpregnant population because there are no studies
including pregnant patients.12 The largest of these is the CALISTO (Comparison of
ARIXTRA in lower LImb Superficial Thrombophlebitis with placebo) trial, a
placebo-controlled trial that found an 85% reduction in subsequent symptomatic
PE, symptomatic DVT, extension to the sapheno-femoral junction, or recurrence for
patients treated for SVT.13 Given that pregnancy itself is a risk factor for VTE, patients
in this group are at higher risk for extension and subsequent PE/DVT and, therefore,
should be considered for prophylactic or therapeutic anticoagulation.
Deep Vein Thrombosis

Presenting symptoms of DVT in pregnancy are similar to those found in the nonpreg-
nant patient with leg pain and swelling as the predominant symptoms. Due to direct
compression of pelvic veins, the left lower extremity is more often involved and iliac
or femoral DVT has a much higher prevalence—approximately 80% of DVTs in preg-
nant patients are proximal compared with less than 20% of nonpregnant patients.14,15
The primary approach to diagnosis remains compression ultrasound. For those pa-
tients with intermediate-to-high probability of disease with a negative or equivocal
compression ultrasound, further imaging with either duplex ultrasonography or venog-
raphy (CT or noncontrast MR) should be pursued. Alternatively, in the right clinical sit-
uation, consideration may be given to empiric treatment. For all patients, 3 to 7 day
follow-up ultrasound is recommended.4
Pulmonary Embolism
Up to 1.5 per 100,000 maternal deaths are due to PE in the United States and Europe,
making PE the leading cause of maternal death in the developed world. Most of these
Cardiovascular Complications of Pregnancy 249
deaths (60%) occur in the postpartum period.16 Delays in diagnosis and treatment,
along with inadequate thromboprophylaxis contribute significantly to these deaths.17
Many of the key clinical features of PE are confounded by the physiologic changes
of pregnancy including tachycardia, tachypnea, dyspnea, and edema. These signs
and symptoms are also incorporated into decision rules, such as modified Well’s
score and revised Geneva score, that are often used to risk stratify nonpregnant pa-
tients for PE. Unfortunately, these decision rules have not been validated in pregnant
patients and studies show they may miss a significant number of PEs even in low-risk
groups, as discussed in the previous edition of this article.18
New Evidence for D-dimer in the Pregnant Patient

The D-dimer test is a frequently used part of the clinical evaluation of PE that obviates
the need for radiologic studies because it has excellent negative predictive value in the
nonpregnant population.19 It represents one of several fibrin degradation products,
which is increased in the serum in the presence of a thrombus. It has been an area
of controversy in the pregnant population because this serum marker increases
throughout pregnancy, creating concern for false positives.
A 2019 study by Van der Pol and colleagues evaluated the YEARS-adjusted D-dimer
algorithm in the setting of pregnancy in a prospective multicenter trial in the
Netherlands. This study included 498 pregnant patients who all received a D-dimer
test. The algorithm suggests PE is unlikely and no imaging is necessary if the D-dimer
is less than 1000 ng/mL and the patient does not meet any of the 3 YEARS criteria:
clinical signs of DVT, hemoptysis, and PE as the most likely diagnosis. In patients
who meet one or more YEARS criteria, it is suggested that PE is unlikely, and imaging
is not necessary if the D-dimer is less than 500 ng/mL. Between both groups that did
not receive imaging, there was 1 DVT found at 3-month follow-up. The overall VTE rate
was low with 20 patients having proven VTE in the study. This approach reduced the
need for imaging by 65% in the first trimester and 32% in the third trimester.20
This study was subsequently incorporated into a systematic review by Bellesini and
colleagues and was the largest of the 4 studies included. This systematic review
included 1194 women from 4 different studies with a low-to-intermediate pretest prob-
ability of PE. The negative predictive value of the D-dimer test in this study was 1.00
with a confidence interval of 0.99 to 1.00. There was significant heterogeneity between
the included studies, and unfortunately, there were few women included in the
highest-risk postpartum period.19 Subsequently, the European Society of Cardiology
in conjunction with the European Respiratory Society recommended D-dimer testing
for patients with low-to-intermediate pretest probability of PE as a means to avoid un-
necessary radiologic testing.7 At this time, this recommendation has, to our knowl-
edge, not been incorporated into any US society guidelines.
The authors of this review agree that a negative D-dimer, particularly in early preg-
nancy, is a reasonable rule-out test in a low-to-intermediate risk group. Since the last
edition of Emergency Medicine Clinics on the topic, the 2 studies above are major new
additions to this area, although further prospective studies are needed, particularly
including postpartum patients.
Imaging for Pulmonary Embolism in Pregnancy

The diagnosis of PE in pregnancy, as in the nonpregnant population, depends on
thoracic imaging using ionizing radiation. Divergent recommendations exist on the
optimal approach to imaging for PE, which are outlined in Table 1.2,4,7
For the patient with lower extremity symptoms or signs of DVT, it is reasonable to
start with ultrasound and proceed to thoracic imaging if negative. If positive, the
250
Sawyer et al
Table 1
Summary of international society guidelines on diagnosis of venous thromboembolism in pregnancy
Use of
Clinical
Decision
Rules (Well’s Use of Ultrasound Before
Geneva)? D-dimer? CTPA for V/Q Scan? CTPA or V/Q?
American College of Obstetrics and No No Unclear Agree with ATS-STR
Gynecology (US)
American Thoracic Society/Society of No No Yes, if LE symptoms CXR (Chest X-ray) then V/Q if normal. If
Thoracic Radiology (US) abnormal, CTPA is reasonable
European Society of Cardiology With D-dimer Yes Yes, if LE symptoms CXR and then either CTPA or V/Q If CXR
abnormal, CTPA
Royal College of Obstetrics and No No Yes, if LE symptoms CXR and then either CTPA or V/Q If CXR
Gynecology (UK) abnormal, CTPA
patient may be initiated on an appropriate anticoagulant drug with a presumptive diag-

nosis of pulmonary embolism. A limited echocardiogram to assess for right heart strain
may be a useful additional study to add to this approach, particularly if the patient is
hemodynamically unstable and being considered for thrombolytic therapy.
Both CT pulmonary angiography (CTPA) and ventilation-perfusion scanning (V/Q)
are reasonable tests for the diagnosis of PE in the pregnant patient.3,21 V/Q scanning
requires a chest radiograph that is normal before proceeding with the study. Tradition-
ally, V/Q scanning has been thought to result in more fetal radiation exposure than
CTPA—although this is somewhat unclear. The CTPA clearly results in more maternal
radiation exposure, particularly to breast tissue, which is particularly sensitive in this
highly proliferative stage of life. The radiation exposure of V/Q scanning can be
reduced by deferring the ventilation portion if the patient has a normal perfusion
scan because this would not be suggestive of PE.3
CTPA has the advantages of elucidating alternate diagnoses, providing information
about right heart strain, and having a lower rate of “nondiagnostic” studies compared
with V/Q scanning.3,22 It is also more readily available at all hours of the day in many
emergency departments. Interestingly, modern CTPA may actually be superior to con-
ventional pulmonary angiography in the non-pregnant population according to the
American College of Radiology.3
A reasonable approach would be to discuss the preferred diagnostic pathway with
your local radiology department and to develop a standardized local protocol before
encountering this emergency department patient.
Treatment
LMWH is the preferred treatment of VTE in pregnancy and postpartum because it does
not cross the placenta and does not cross into breast milk. The American Society of
Hematology guidelines recommend LMWH with either once daily or twice daily
dosing. The patient should have close subspecialty follow-up because the increased
volume of distribution associated with the normal hypervolemia of pregnancy may
affect serum levels. For patients with severe renal dysfunction, unfractionated heparin
is the preferred treatment.12 For the patient who is peripartum or periprocedural, a
heparin drip may be preferred due to the ability to stop the infusion with rapid return
to normal clotting parameters.4,7
Rarely a patient with a severe heparin allergy may be encountered. Although there is
little evidence in this area, treatment with fondaparinux is recommended.4,7
Warfarin is generally not recommended in the pregnant or postpartum patient
because it has known teratogenic effects and crosses into breast milk. Direct oral an-
ticoagulants (DOACs) including the factor Xa inhibitors and direct thrombin inhibitors
are not recommended in pregnancy due to a lack of evidence on safety and efficacy.4
In postpartum patients, evidence for safety of DOACs is also lacking and there is some
evidence it may cross into breast milk.12
For patients with hemodynamic instability due to PE, treatment with thrombolytic
therapy is recommended.4,7,12,23 For patients with evidence of right heart strain but
who have not developed hemodynamic instability, thrombolytic therapy is not recom-
mended.12 Finally, for the crashing pregnant patient with PE extracorporeal mem-
brane oxygenation (ECMO), if available, may be considered as a risky but
necessary intervention.
In any patient with confirmed or ongoing concern for VTE, multidisciplinary involve-
ment and/or close follow-up should be obtained. Carefully selected patients with DVT
may be candidates for outpatient treatment. Most patients with confirmed PE will be
admitted for management.
252 Sawyer et al
ACUTE MYOCARDIAL INFARCTION
Acute myocardial infarction (AMI) complicates approximately 3 per 100,000 pregnan-

cies worldwide. However, in the United States, AMI complicates nearly 5 per 100,000
pregnancies and is associated with a higher maternal mortality rate.24 Pregnancy itself
is an independent risk factor for myocardial infarction with a 3-fold to 4-fold increase in
risk.25 Pregnancy-specific conditions such as eclampsia and preeclampsia also in-
crease the risk of subsequent AMI. With the increasing prevalence of cardiovascular
comorbidities and advanced maternal age, this problem may only grow as a significant
contributor to the increasing cardiovascular deaths associated with pregnancy. The
overall mortality from AMI in pregnancy is around 5%.24–26
Due to the increasing physiologic stresses throughout pregnancy, it is unsurprising
that the incidence of AMI, although reported in all stages, increases throughout the
course of pregnancy, with the highest risk in the peripartum and postpartum pe-
riods.24,25,27 Pregnant women experience anemia due to a relative hemodilution,
which occurs in spite of increased red blood cell mass and in turn compromises
myocardial oxygen delivery. Myocardial oxygen demand is also increased because
of increased stroke volume and heart rate.
The clinical presentation of AMI in pregnancy and postpartum includes chest pain,
dyspnea, nausea, vomiting, and diaphoresis. Unfortunately, as discussed previously,
pregnant women experience exertional dyspnea and fatigue that may be difficult to
differentiate as physiologic versus pathologic cardiac symptoms.
The diagnostic approach is the same as in the nonpregnant patient and hinges on
electrocardiogram (EKG) changes and elevated serum markers. An EKG should be
obtained and, if ST-elevation myocardial infarction (STEMI) criteria are present, an
emergent cardiac catheterization will be necessary to elucidate the diagnosis. A
troponin level may also be suggestive of AMI but there is the possibility of an elevated
troponin without the presence of coronary disease in the setting of preeclampsia or
gestational hypertension.28 In the case of AMI found to be due to plaque rupture or
thrombosis, percutaneous coronary intervention (PCI) remains the treatment of
choice. However, a significant number of pregnancy-associated AMIs are due to
spontaneous coronary artery dissection (SCAD), which may be managed differently,
as outlined below. Aspirin, nitrates, beta-blockers, and heparin are all considered
safe in pregnancy and may be part of the emergency department treatment of the
pregnant patient with AMI. The caveat for heparin, that is discussed below, is that
there is a high prevalence of SCAD in this population.
Spontaneous Coronary Artery Dissection

SCAD accounts for up to 43% of pregnant patients presenting with STEMI and
seems to occur in 1.8 per 100,000 pregnancies, making it the most common cause
of AMI in this population.29,30 SCAD is thought to occur secondary to weakened
vessel walls, which leads to either an intramural hematoma that ruptures or an intimal
flap that propagates and forms a false lumen.31 The hormonal changes of pregnancy
and hemodynamic stress applied to the vasculature are thought to predispose to
SCAD. Traditional risk factors for SCAD include advanced maternal age, smoking
history, hypertension, and diabetes.31 Nonetheless, SCAD in the setting of preg-
nancy has been reported in many patients without these traditional risk factors for
coronary artery disease. When compared with nonpregnant patients with SCAD, it
seems that pregnant patients present more critically ill with a higher incidence of
STEMI, proximal dissection, multivessel involvement, decreased LV systolic function,
and cardiogenic shock.27,31 SCAD generally occurs in the left main or left anterior
descending circulation.27,31 Patients generally present with chest pain, and it most
often occurs in late pregnancy or in the early postpartum period.27 This diagnosis
is made in the catheterization suite by the interventionalist but awareness of this
clinical condition is important for the emergency clinician because there are
significant changes in the approach to treating SCAD. Notable changes are outlined
below.
Glycoprotein IIb/IIIa inhibitors are not recommended because they may increase
the risk of propagation and bleeding.31
Thrombolytics are not recommended because they may also further increase the
risk of propagation of the false lumen.31 Therefore, given the high prevalence of
SCAD in this population, these patients should be transferred to a center with
cardiac catheterization, if possible.
Although the diagnosis is made by conventional coronary angiography, subse-
quent PCI is often less desirable unless the patient has refractory symptoms, re-
fractory arrhythmias, or cardiogenic shock.
Coronary artery bypass grafting is also an option in some of these patients with a
better short-term outcome than PCI but with higher longer term graft failure than
CABG in non-SCAD patients.31
The American Heart Association recommends that patients found to have SCAD are
preferentially treated medically with beta-blocker, long-term aspirin, short-term clopi-
dogrel, and with the addition of a statin in patients with dyslipidemia.32,33 The emer-
gency clinician managing a pregnant patient meeting STEMI criteria will not know
the underlying cause and, thus, should consider administering heparin and other anti-
platelets in conjunction with cardiology recommendations.
PERIPARTUM CARDIOMYOPATHY
Peripartum cardiomyopathy (PPCM) is a consideration in any patient in the later

stages of pregnancy or postpartum who presents with dyspnea. It was formerly
called postpartum cardiomyopathy and included any patient who developed idio-
pathic systolic heart failure within 5 months of delivery. However, the definition has
been expanded to include patients who present in the last month of pregnancy
with systolic heart failure.34 As with the other entities discussed in this article, the
presentation is confounded by significant symptomatic overlap with the normal phys-
iologic changes of pregnancy and with other important disorders such as preeclamp-
sia. Cardiomyopathy is a significant cause of pregnancy-related mortality, accounting
for approximately 11% of deaths.1 For patients with PPCM, the mortality rate is up to
28% with a mean mortality of 16%. A significant number of these patients also have a
diagnosis of preeclampsia (w30%).35 The signs and symptoms of PPCM include
dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, edema, pulmonary
rales, elevated jugular venous pressure, and chest tightness among others. With
severely depressed ejection fraction, these patients may present in cardiogenic
shock or with thromboembolic complications. Delays in diagnosis result in worse
outcomes.34
The diagnosis of PPCM is one of exclusion and so is unlikely to be made in the emer-
gency department before the exclusion of alternate causes (CAD, preexisting cardiac
disease, hypertensive disorders of pregnancy, valvular disease, and so forth). The
workup includes EKG, chest radiograph, troponin, and brain-natriuretic peptide. An
echocardiogram will also be part of the workup and an emergency department
bedside echocardiogram may be helpful in ruling in the diagnosis.
254 Sawyer et al
The management of PPCM is similar to that of heart failure in nonpregnant patients,

including the use of noninvasive ventilation strategies, with a few exceptions.28
During pregnancy, angiotensin converting enzyme (ACE) inhibitors, angiotensin
receptor blockers and aldosterone antagonists are contraindicated.
Diuretics may be initiated in patients with adequate SBP with the caveat that they
may cause decreased placental blood flow.
If afterload reduction is required, nitroprusside is contraindicated during preg-
nancy. However, the use of nitroglycerin is acceptable.
Bromocriptine is an experimental treatment of patients with a previous diagnosis
of PPCM.
For patients with thromboembolic complications, heparin or LMWH is the
preferred anticoagulation medication. Warfarin is contraindicated in pregnancy
and breastfeeding.
Early delivery through C-section may be indicated if the fetus is viable.
The principle of management for the critically ill pregnant patient remains supporting
the hemodynamics of the mother because this is the most important factor influencing
fetal survival. Norepinephrine and other vasopressors and inotropes are not thor-
oughly studied in pregnancy but should be used if necessary.28 Other treatments
such as mechanical circulatory support, ECMO, and implantable cardiac defibrillator
(ICD) implantation may be indicated. Early involvement of obstetrics, cardiology, and
critical care are paramount. Many women will ultimately have a full recovery but the
course may be prolonged.
AORTIC DISSECTION
Pregnancy itself is thought to be an independent risk factor for aortic dissection,

although this remains an extremely rare event, making definitive conclusions
elusive.36,37 The largest study of pregnancy-related aortic dissection included 44 to-
tal cases during a 20-year period, which accounted for 0.1% of all reported aortic
dissections. Based on this, the resulting incidence of aortic dissection in all pregnan-
cies is 0.0004%.38 The increased cardiac output, due to both increased heart rate
and stroke volume, produces more stress on the aortic walls allowing for the prop-
agation of the dissection. Hormonal changes are thought to drive the histopathologic
changes in the aortic intima and media that classically predispose to an intimal
tear.38–40 These vascular changes may actually persist for up to 12 months post-
partum.40 The most common risk factor identified for pregnancy-related aortic
dissection seems to be preexisting aortopathy (Marfan syndrome, Loeys-Dietz syn-
drome, and other connective tissue disorders) or bicuspid aortic valve but most of
these women are unfortunately unaware of their condition before pregnancy.41 The
incidence of aortic dissection, as with the other cardiovascular conditions covered
in this article, seems to increase throughout pregnancy and peaks in the early post-
partum period.41
Regarding the clinical presentation of aortic dissection in pregnancy, the most com-
mon presenting symptom remains chest pain, although it is not universally present.42
Unfortunately, as with the nonpregnant patient, there is often a missed diagnosis or
delay to diagnosis at initial presentation, which may be expected given the much
higher incidence of alternate causes of chest pain.43,44 Other presenting symptoms
include syncope, nausea, vomiting, shortness of breath, and neurologic deficits. A
delay to diagnosis is particularly concerning given the estimated hourly increase of
1% to 2% mortality. Although pregnancy-related changes confound the presentation,
a detailed history and physical focusing on the quality of pain, radiation of pain, asso-
ciated symptoms, new murmurs, and pulse differences are key to increasing the index
of suspicion and ruling in the diagnosis.45
The diagnostic tests of choice for aortic dissection in the pregnant patient are the
same as those in the nonpregnant patient. Due to widespread availability, high sensi-
tivity, and high specificity, CT angiography of the aorta is the most commonly used
test in the emergency department.46 Trans-esophageal echocardiography (TEE)
also has high sensitivity and specificity for thoracic aortic dissection and, if available,
is a viable option that has the benefit of sparing exposure to radiation.46 In an institu-
tion where cardiac anesthesiologists or cardiologists trained in TEE are in-house,
consider requesting bedside TEE to confirm the diagnosis in unstable patients in
the emergency department (ED) with thoracic aortic dissection. Finally, magnetic
resonance (MR) aortography, while highly sensitive and specific, may not be useful
in the pregnant patient. First, MR has limited availability in most hospitals, with the
additional downside of taking a potentially unstable patient away from the emergency
department for an extended period. Second, the most commonly available MR aorta
protocols rely on administration of gadolinium contrast, which is contraindicated in
pregnancy and relatively contraindicated in the breast-feeding mother.
Type A Stanford aortic dissection, involving the ascending aorta or arch, seems to
account for w67% of pregnancy-related aortic dissections.47 As with the nonpregnant
patient, early surgical consultation and intervention is key in the treatment of Type A
aortic dissections. The surgical intervention of choice in later pregnancy is Caesarean
section followed by immediate surgical repair of the aorta in the same opera-
tion.44,47–49 Unfortunately, the maternal mortality seems to be up to 23%, whereas
the fetal/neonatal mortality is 27% to 33%.39,50
For Type B Stanford aortic dissection, early surgical consultation is advised as well,
although the need for surgical intervention depends on the clinical scenario. In both
types of aortic dissection, emergency department management involves maternal
cardiovascular control with vasoactive infusions, fetal heart rate monitoring, and early
obstetric consultation. A heart rate goal of w60 beats per minute should be targeted
first using beta-blocker infusions, most commonly esmolol. After heart rate control has
been achieved, afterload reduction with a goal systolic blood pressure (SBP) of less
than 110 mm Hg should be targeted using calcium channel blocker infusion, most
commonly nicardipine. It should be noted that ACE inhibitors and nitroprusside are
contraindicated in pregnancy. For the patient that presents with shock, either due
to acute aortic regurgitation, pericardial tamponade, or hemorrhage, a shift in focus
to blood pressure support may be required.
CLINICS CARE POINTS
When working up a pregnant patient for low-risk to intermediate probability VTE, applying
the pregnancy-adjusted YEARS algorithm with D-dimer test is an emerging option that may
reduce the need for further imaging.
When evaluating a pregnant patient with STEMI, SCAD is a significant pathophysiologic
mechanism in this population. Therefore, in the setting of STEMI in this population,
routine administration of heparin is not recommended.
The preferred anticoagulant in pregnancy, whether for VTE or other thrombotic
complications, is heparin or LMWH. Warfarin is contraindicated in pregnancy, and DOACs
are not well studied in pregnancy.
256 Sawyer et al
DISCLOSURES
None of the authors of this article has any commercial or financial conflicts of interest
to disclose.
REFERENCES
1. Creanga AA, Syverson C, Seed K, et al. Pregnancy-Related Mortality in the

United States, 2011-2013. Obstet Gynecol 2017;130(2):366–73.
2. Leung AN, Bull TM, Jaeschke R, et al. American Thoracic Society documents: an
official American Thoracic Society/Society of Thoracic Radiology Clinical Practice
Guideline–Evaluation of Suspected Pulmonary Embolism in Pregnancy. Radi-
ology 2012;262(2):635–46.
3. Expert Panels on Cardiac and Thoracic I, Kirsch J, Brown RKJ, et al. ACR Appro-
priateness Criteria Acute Chest Pain-Suspected Pulmonary Embolism. J Am
Coll Radiol: JACR 2017;14(5S):S2–12.
4. American College of Obstetricians and Gynecologists’ Committee on Practice
BO. ACOG Practice Bulletin No. 196: Thromboembolism in Pregnancy. Obstet
Gynecol 2018;132(1):e1–17.
5. American College of Emergency Physicians Clinical Policies Subcommittee on
Thromboembolic D, Wolf SJ, Hahn SA, et al. Clinical Policy: Critical Issues in
the Evaluation and Management of Adult Patients Presenting to the Emergency
Department With Suspected Acute Venous Thromboembolic Disease. Ann
Emerg Med 2018;71(5):e59–109.
6. Cohen SL, Feizullayeva C, McCandlish JA, et al. Comparison of international so-
cietal guidelines for the diagnosis of suspected pulmonary embolism during
pregnancy. Lancet Haematology 2020;7(3):e247–58.
7. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diag-
nosis and management of acute pulmonary embolism developed in collaboration
with the European Respiratory Society (ERS). Eur Heart J 2020;41(4):543–603.
8. Heit JA, Kobbervig CE, James AH, et al. Trends in the incidence of venous throm-
boembolism during pregnancy or postpartum: a 30-year population-based study.
Ann Intern Med 2005;143(10):697–706.
9. Galanaud JP, Bosson JL, Genty C, et al. Superficial vein thrombosis and recurrent
venous thromboembolism: a pooled analysis of two observational studies.
J Thromb Haemostasis: JTH 2012;10(6):1004–11.
10. Scovell SD, Ergul EA, Conrad MF. Medical management of acute superficial vein
thrombosis of the saphenous vein. Journal of Vascular Surgery Venous and
Lymphatic Disorders 2018;6(1):109–17.
11. Stevens SM, Woller SC, Baumann Kreuziger L, et al. Executive Summary: Antith-
rombotic Therapy for VTE Disease: Second Update of the CHEST Guideline and
Expert Panel Report. Chest 2021;160(6):2247–59.
12. Bates SM, Rajasekhar A, Middeldorp S, et al. American Society of Hematology
2018 guidelines for management of venous thromboembolism: venous thrombo-
embolism in the context of pregnancy. Blood Advances 2018;2(22):3317–59.
13. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of
superficial-vein thrombosis in the legs. N Engl J Med 2010;363(13):1222–32.
14. Chan W-S, Spencer FA, Ginsberg JS. Anatomic distribution of deep vein throm-
bosis in pregnancy. CMAJ (Can Med Assoc J): Canadian Medical Association
journal 2010;182(7):657–60.
15. Bukhari S, Fatima S, Barakat AF, et al. Venous thromboembolism during preg-
nancy and postpartum period. Eur J Intern Med 2022;97:8–17.
16. Abe K, Kuklina EV, Hooper WC, et al. Venous thromboembolism as a cause of se-
vere maternal morbidity and mortality in the United States. Semin Perinatol 2019;
43(4):200–4.
17. Marik PE, Plante LA. Venous thromboembolic disease and pregnancy. N Engl J
Med 2008;359(19):2025–33.
18. Borhart J, Palmer J. Cardiovascular Emergencies in Pregnancy. Emerg Med Clin
2019;37(2):339–50.
19. Bellesini M, Robert-Ebadi H, Combescure C, et al. D-dimer to rule out venous
thromboembolism during pregnancy: A systematic review and meta-analysis.
J Thromb Haemostasis 2021;19(10):2454–67.
20. van der Pol LM, Tromeur C, Bistervels IM, et al. Pregnancy-Adapted YEARS Al-
gorithm for Diagnosis of Suspected Pulmonary Embolism. N Engl J Med 2019;
380(12):1139–49.
21. van Mens TE, Scheres LJ, de Jong PG, et al. Imaging for the exclusion of pulmo-
nary embolism in pregnancy. Cochrane Database Syst Rev 2017;1:CD011053.
22. Sadeghi S, Arabi Z, Moradi M, et al. Diagnostic imaging to investigate pulmonary
embolism in pregnancy using CT-Pulmonary angiography versus perfusion scan.
J Res Med Sci 2021;26:37.
23. Martillotti G, Boehlen F, Robert-Ebadi H, et al. Treatment options for severe pul-
monary embolism during pregnancy and the postpartum period: a systematic re-
view. J Thromb Haemostasis 2017;15(10):1942–50.
24. Gibson P, Narous M, Firoz T, et al. Incidence of myocardial infarction in preg-
nancy: a systematic review and meta-analysis of population-based studies. Euro-
pean Heart Journal Quality of Care & Clinical Outcomes 2017;3(3):198–207.
25. James AH, Jamison MG, Biswas MS, et al. Acute myocardial infarction in preg-
nancy: a United States population-based study. Circulation 2006;113(12):
1564–71.
26. Ladner HE, Danielsen B, Gilbert WM. Acute myocardial infarction in pregnancy
and the puerperium: a population-based study. Obstet Gynecol 2005;105(3):
480–4.
27. Tweet MS, Hayes SN, Codsi E, et al. Spontaneous Coronary Artery Dissection
Associated With Pregnancy. J Am Coll Cardiol 2017;70(4):426–35.
28. Bauersachs J, König T, van der Meer P, et al. Pathophysiology, diagnosis and
management of peripartum cardiomyopathy: a position statement from the Heart
Failure Association of the European Society of Cardiology Study Group on peri-
partum cardiomyopathy. Eur J Heart Fail 2019;21(7):827–43.
29. Elkayam U, Jalnapurkar S, Barakkat MN, et al. Pregnancy-associated acute
myocardial infarction: a review of contemporary experience in 150 cases be-
tween 2006 and 2011. Circulation 2014;129(16):1695–702.
30. Faden MS, Bottega N, Benjamin A, et al. A nationwide evaluation of spontaneous
coronary artery dissection in pregnancy and the puerperium. Heart. British Car-
diac Society) 2016;102(24):1974–9.
31. Hayes SN, Kim ESH, Saw J, et al. Spontaneous Coronary Artery Dissection: Cur-
rent State of the Science: A Scientific Statement From the American Heart Asso-
ciation. Circulation 2018;137(19):e523–57.
32. Saw J, Aymong E, Sedlak T, et al. Spontaneous coronary artery dissection: asso-
ciation with predisposing arteriopathies and precipitating stressors and cardio-
vascular outcomes. Circulation Cardiovascular Interventions 2014;7(5):645–55.
33. Saw J. Spontaneous coronary artery dissection. Can J Cardiol 2013;29(9):
1027–33.
258 Sawyer et al
34. Davis MB, Arany Z, McNamara DM, et al. Peripartum Cardiomyopathy: JACC
State-of-the-Art Review. J Am Coll Cardiol 2020;75(2):207–21.
35. Asad ZUA, Maiwand M, Farah F, et al. Peripartum cardiomyopathy: A systematic
review of the literature. Clin Cardiol 2018;41(5):693–7.
36. Nasiell J, Lindqvist PG. Aortic dissection in pregnancy: the incidence of a life-
threatening disease. Eur J Obstet Gynecol Reprod Biol 2010;149(1):120–1.
37. Kamel H, Roman MJ, Pitcher A, et al. Pregnancy and the Risk of Aortic Dissection
or Rupture: A Cohort-Crossover Analysis. Circulation 2016;134(7):527–33.
38. Sawlani N, Shroff A, Vidovich MI. Aortic dissection and mortality associated with
pregnancy in the United States. J Am Coll Cardiol 2015;65(15):1600–1.
39. De Martino A, Morganti R, Falcetta G, et al. Acute aortic dissection and preg-
nancy: Review and meta-analysis of incidence, presentation, and pathologic sub-
strates. J Card Surg 2019;34(12):1591–7.
40. Rommens KL, Sandhu HK, Miller CC, et al. In-hospital outcomes and long-term
survival of women of childbearing age with aortic dissection. J Vasc Surg
2021;74(4):1135–42.e1.
41. Braverman AC, Mittauer E, Harris KM, et al. Clinical Features and Outcomes of
Pregnancy-Related Acute Aortic Dissection. JAMA cardiology 2021;6(1):58–66.
42. Meng X, Han J, Wang L, et al. Aortic dissection during pregnancy and post-
partum. J Card Surg 2021;36(7):2510–7.
43. Lameijer H, Crombach A. Aortic Dissection During Pregnancy or in the Post-
partum Period: It All Starts With Clinical Recognition. Ann Thorac Surg 2018;
105(2):663.
44. Ch’ng SL, Cochrane AD, Goldstein J, et al. Stanford type a aortic dissection in
pregnancy: a diagnostic and management challenge. Heart Lung Circ 2013;
22(1):12–8.
45. Rosman HS, Patel S, Borzak S, et al. Quality of history taking in patients with
aortic dissection. Chest 1998;114(3):793–5.
46. Expert Panel on Cardiac I, Kicska GA, Hurwitz Koweek LM, et al. ACR Appropri-
ateness Criteria Suspected Acute Aortic Syndrome. J Am Coll Radiol: JACR
2021;18(11S):S474–81.
47. Aziz F, Penupolu S, Alok A, et al. Peripartum acute aortic dissection: A case
report & review of literature. J Thorac Dis 2011;3(1):65–7.
48. Yam N, Lo CS-Y, Ho CK-L. Acute Aortic Dissection Associated With Pregnancy.
Ann Thorac Surg 2015;100(4):1470.
49. Rimmer L, Heyward-Chaplin J, South M, et al. Acute aortic dissection during
pregnancy: Trials and tribulations. J Card Surg 2021;36(5):1799–805.
50. Jha N, Jha AK, Chand Chauhan R, et al. Maternal and Fetal Outcome After Car-
diac Operations During Pregnancy: A Meta-Analysis. Ann Thorac Surg 2018;
106(2):618–26.

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C a rd i o v a s c u l a r

Emerg Med Clin N Am 41 (2023) 247–258

VENOUS THROMBOEMBOLISM IN PREGNANCY

Superficial Vein Thrombosis

Deep Vein Thrombosis

New Evidence for D-dimer in the Pregnant Patient

Imaging for Pulmonary Embolism in Pregnancy

patient may be initiated on an appropriate anticoagulant drug with a presumptive diag-

ACUTE MYOCARDIAL INFARCTION

Acute myocardial infarction (AMI) complicates approximately 3 per 100,000 pregnan-

Spontaneous Coronary Artery Dissection

Peripartum cardiomyopathy (PPCM) is a consideration in any patient in the later

The management of PPCM is similar to that of heart failure in nonpregnant patients,

Pregnancy itself is thought to be an independent risk factor for aortic dissection,

CLINICS CARE POINTS

1. Creanga AA, Syverson C, Seed K, et al. Pregnancy-Related Mortality in the

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